首页|Role of the receptor for advanced glycation end products in hepatic fibrosis

Role of the receptor for advanced glycation end products in hepatic fibrosis

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  • NSTL
  • Baishideng Publishing Group Inc
AIM: To study the role of advanced glycation end products (AGE) and their specific receptor (RAGE) in the pathogenesis of liver fibrogenesis.METHODS: In vitro RAGE expression and extracellular matrix-related gene expression in both rat and human hepatic stellate cells (HSC) were measured after stimulation with the two RAGE ligands, advanced glycation end product-bovine serum albumin (AGE-BSA) and N~ε-(carboxymethyl) lysine (CML)-BSA, or with tumor necrosis factor-α (TNF-α). In vivo RAGE expression was examined in models of hepatic fibrosis induced by bile duct ligation or thioacetamide. The effects of AGE-BSA and CML-BSA on HSC proliferation, signal transduction and profibrogenic gene expression were studied in vitro.RESULTS: In hepatic fibrosis, RAGE expression was enhanced in activated HSC, and also in endothelial cells, inflammatory cells and activated bile duct epithelia. HSC expressed RAGE which was upregulated after stimulation with AGE-BSA, CML-BSA, and TNF-α.RAGE stimulation with AGE-BSA and CML-BSA did not alter HSC proliferation, apoptosis, fibrogenic signal transduction and fibrosis- or fibrolysis-related gene expression, except for marginal upregulation of procollagen α1(I) mRNA by AGE-BSA.CONCLUSION: Despite upregulation of RAGE in activated HSC, RAGE stimulation by AGE does not alter their fibrogenic activation. Therefore, RAGE does not contribute directly to hepatic fibrogenesis.

advanced glycation end productextracellular matrixhepatic stellate cellmatrix metalloproteinasemyofibroblastreceptor for advanced glycation end productstransforming growth factor βtissue inhibitor of metalloproteinasetumor necrosis factor α

Christina Lohwasser、Daniel Neureiter、Yury Popov、Michael Bauer、Detlef Schuppan

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Department of Medicine I, University of Erlangen-Nuremberg, Erlangen-Nuernberg, D-91054, Germany

Institute of Pathology, Paracelsus Private Medicine University, Salzburg, A-5020, Austria

Department of Medicine I, University of Erlangen-Nuremberg, Erlangen-Nuernberg, D-91054, Germany Division of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States

Department of Medicine I, University of Erlangen-Nuremberg, Erlangen-Nuernberg, D-91054, GermanyDivision of Gastroenterology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, United States Division of Gastroenterology, Beth Israel-Deaconess Medical Center and Harvard Medical School, 330 Brookline Avenue, Dana 506, Boston, MA 02215, United States

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2009

10.3748/wjg.15.5789

World Journal of Gastroenterology: WJG

World Journal of Gastroenterology: WJG

ISTP
ISSN：1007-9327
年,卷(期)：2009.15(46)
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